A possible acetaldehyde-mediated cardioprotective mechanism.

Excess alcohol consumption may affect the cardiovascular system in various ways. Adverse effects include hypertension (McMahon, 1987), arrhythmias (Ettinger et al, 1978), cardiomyopathy (Urbano-Marquez et al, 1989) and haemorrhagic stroke (Camargo, 1989). One beneficial effect of moderate alcohol consumption appears to be some protection against morbidity and mortality from coronary heart disease. This effect has been attributed to a number of mechanisms. These include an increase in the reverse transport of cholesterol as a consequence of increased levels of high density lipoprotein (Gaziano et al, 1993), decreased ADP-, collagenand adrenaline-induced aggregability of platelets (Renaud et al., 1981; Pikaar et al., 1987; Veenstra et al., 1990; Thaulow et al, 1991), effects on the fibrinolytic system (Veenstra, 1990) and the potentially anti-atherogenic action of antioxidants in red wine (Witztum, 1994; Maxwell et al, 1994). Another possible mechanism stems from a report that acetaldehyde (10-100 uM) stimulates rat aortic rings to produce prostacyclin (PGI2) which is both a potent vasodilator and a potent inhibitor of platelet aggregation (Guivernau et al, 1987). However, this study did not determine whether prostacyclin release was from endothelial cells, smooth muscle cells or both. We have therefore investigated whether ethanol, acetaldehyde or acetaldehyde-albumin complexes found in serum after alcohol consumption influence prostacyclin release from cultured human umbilical vein-derived endothelial cells.